MANAGEMENT OF COMMON PAIN SYNDROME

1. MANAGEMENT OF COMMON PAIN
SYNDROME;
NEUROPATHIC PAIN SYNDROME
BY DOREEN G. GALON, MD
2ND YR RESIDENT
Preceptors:
Dr. Ruel Trivilegio
Dr. Rosalie Iturriaga
Dr. Mayflor Altamira

2. COMMON PAIN
SYNDROMES

3. Common Pain Syndromes
Low Back Pain
Radicular
Pain
Syndrome
Facet
Syndrome
Buttock Pain
Sacroiliac
Joint
Syndrome
Piriformis
Syndrome
Myofascial
Pain Syndrome
Fibromyalgia

4. Low Back Pain: Radicular pain
Syndromes
• Radicular
symptoms
• Pain
• Paresthesia
• Numbness
• Weakness
• Diminished
reflexes
• Positive
straight-leg
raise
Pathology or
dysfunction of
the sensory
spinal nerve
roots

5. Low Back Pain: Radicular pain Syndromes
• Low back and radicular pain secondary to a herniated disc
 due to mechanical nerve root compression and the subsequent inflammatory process
 Chemical radiculitus – results when there is a local release of cytokines and
inflammatory mediators secondary to an herniated nucleus pulposus
 Inc phospholipase A2 activity
 Inc levels of interleukin-6 and interleukin-8
• The application of disc material onto spinal nerve roots can induce functional and
morphologic changes in the nerves.
• Disc cells express TNF-α;
• selective inhibition of TNF-α may reduce the intraneural edema

6. SYMPTOMATIC HERNIATED DISC
• Low back pain
• Radicular symptoms: paresthesia, numbness, and weakness in the distribution of the
involved nerve root
• Gait disturbances
• Loss of sensation
• Reduced muscle strength
• Diminished reflexes

7. Treatment
• Asymptomatic: spontaneous regression, medications, bed rest, physical therapy,
traction, or epidural steroids
• Patients with radicular symptoms:
• epidural steroid injections (ESIs)
• inhibition of phospholipase A2 activity,
• Antinociceptive
• more effective in patients with acute radicular symptoms
• Gabapentin
• Duloxetine

8. Transforaminal approach (ESIs)
• steroid is deposited in the anterolateral epidural space, where the herniated disc is
located, through the intervertebral foramina, and distally along the nerve root
• indicated in radicular pain specific to a single nerve root
• Studies showed better efficacy than the midline interlaminar approach
• Fluoroscopy is used
• Reassessment after 2-3 weeks of initial injection

9. Complications of ESI
• Needle trauma, vasospasm, infection
• Impaired Insulin sensitivity
• Injury to the brain or spinal cord – transforaminal ESIs
• Vertebral artery trauma
• vasospasm from the injected steroid or dye, or
• embolism of the particulate steroid via the vertebral artery
• Radicular artery injury
• injury to the radicular artery accompanying the nerve root,
• spasm from the injected dye or steroid, or
• embolism of the particulate steroid
• intra-arterial injection into an abnormally low-lying artery of Adamkiewicz – lumbar
level

10. Recommendations to improve the safety of ESIs
1. Interlaminar ESIs should be performed using image guidance with appropriate
anteroposterior, lateral, or contralateral oblique views, and contrast media.
2. Cervical interlaminar ESI should be performed at C6-C7 or C7-T1 but not higher.
3. Transforaminal ESIs should be performed by injecting contrast medium under
real-time fluoroscopy and/or digital subtraction imaging, using an AP view,
before injection.
4. Particulate steroids should not be used in therapeutic cervical transforaminal
(TF) ESIs.
5. Nonparticulate steroid (dexamethasone) should be used in initial TF ESIs.
6. There are situations where a particulate steroid can be used in lumbar TF ESIs.

11. Low Back Pain: Facet Syndrome
• pain in the low back that radiates to the ipsilateral posterior thigh and usually ends
at the knee
• PE: paraspinal tenderness and reproduction of pain with extension–rotation
maneuvers of the back
• Diagnosis: history, physical examination findings, and a positive response to
diagnostic medial branch blocks or facet joint injections

12. Treatment
• Medial branch block - use local anesthetics with different durations of effect
(e.g., lidocaine and bupivacaine), then correlate the duration of relief with the
known duration of effect of the drug.
• Prolonged response: up to 3 to 6 months
• If relief is short-lived: thermal radiofrequency (RF) rhizotomy of the medial
branches
• thermal RF of the lumbar medial branches lasted 3 to 12 months
• cervical facet syndrome - majority of the patients were pain free at 6 months and over
one-third were pain-free at 1 year

13. Buttock Pain: Sacroiliac Joint Syndrome
• Location: region of the affected sacroiliac joint and the medial buttock
• pain may radiate to the groin, posterior thigh, and occasionally below the knee
• PE: tenderness over the sacroiliac sulcus, reduction in the joint mobility, and
reproduction of the pain when the affected sacroiliac joint is stressed
• Most commonly used tests for sacroiliac joint dysfunction:
• FABER (flexion, abduction and external rotation), or Patrick test, and the Gaenslen,
Yeoman, sacroiliac shear, and Gillet tests
• FABER (Patrick) and Yeoman test: do not rule out hip pathology
• Yeoman and shear tests: more specific for sacroiliac joint syndrome

14. Diagnosis
• presence of symptoms and physical examination findings suggestive of sacroiliac
(SI) joint syndrome,
• pain on three of the provocative tests,
• positive response to SI joint injection

15. Treatment
• Physical therapy,
• Chiropractic manipulation,
• Intra-articular steroid injections - (40 to 80 mg of methylprednisolone or other
depot steroid) and local anesthetic
• RF denervation of the lower portion of the SI joint - achieved by the creation of
bipolar RF strip lesions along the dorsal border of the SI joint in a leapfrog manner
• multilesion probe (Simplicity III, NeuroTherm) along the posterior sacral plate lateral to
the foraminas can be effective for at least 6 months
• Local anesthetic blockade of the sensory innervation of the dorsal portion of the SI
joint—the medial branch of the dorsal rami of L5 and the lateral branches of the dorsal
rami of S1 to S3
• Surgical fusion of the joint

16. Buttock Pain: Piriformis Syndrome
• occurs after trauma, surgery, and infection, or from compression of one of the
components of the sciatic nerve as it runs between two divisions of the piriformis
muscle
• Symptoms: buttock pain with or without radiation to the ipsilateral leg
• The pain is aggravated by hip flexion, adduction, and internal rotation.
• Neurologic examination - negative.
• (+) leg numbness - sciatic nerve is irritated
• Straight-leg test may be normal or limited
• Electromyography – detect myopathic and neuropathic changes

17. Three signs confirm the presence
of piriformis syndrome
1. Pace sign - pain and weakness on resisted abduction of the hip in
a patient who is seated with the hip flexed
2. Lasègue sign (Pain on straight-leg raise) - pain on flexion,
adduction, and internal rotation of the hip in a patient who is
supine
3. Freiberg sign - pain on forced internal rotation of the extended
thigh
 Note that the piriformis is an internal rotator of the flexed hip and
an external rotator of the extended hip

18. Treatment
• physical therapy combined with medications such as muscle relaxants, anti-
inflammatory drugs, and analgesics to reduce the spasm, inflammation, and pain
• Local anesthetic and steroid injections into the piriformis muscle may break the
pain/muscle spasm cycle
• use of CT guidance, use of a nerve stimulator, or combined fluoroscopy–nerve stimulator
guidance
• 100 units of botulinum toxin A in 2 to 3 mL of local anesthetic – if relief from local
anesthetic does not last

19. Myofascial Pain Syndrome
• painful regional syndrome characterized by the presence of an active trigger point
in a skeletal muscle
• Trigger point – palpable taut band
• Manipulation of the trigger point by digital pressure or by penetration by a needle
may induce a twitch response
• (+) spot tenderness in the taut band
• (+) experienced pain pattern – pain upon pressure on the tender nodule
• (+) limitation to full passive range of motion of the affected muscle

20. Treatment
• Repeated applications of a cold spray over the trigger point in line with the
involved muscle fibers, followed by gentle massage of the trigger point and
stretching of the affected muscle
• Physical therapy
• improving posture, body mechanics, relaxation techniques, trigger point massage,
postisometric relaxation, and reciprocal inhibition.
• Local anesthetic injection or dry needling of the trigger point
• Several injections at 2- to 3-week intervals, followed by physical therapy, may result in a
long-term benefit
• Botulinum toxin injections

21. Fibromyalgia
• American College of Rheumatology criteria for classification of fibromyalgia
(1990):
• a history of widespread pain for at least 3 months
• allodynia to digital pressure at 11 or more of 18 anatomically defined tender points
• Tender points:
• occiput,
• the intertransverse spaces between C5 and C7,
• trapezii,
• supraspinatus,
• the second rib (just lateral to the costochondral junctions),
• lateral epicondyles,
• glutei,
• greater trochanters,
• knees.

22. Diagnosis
• 2010: new diagnostic paradigm was proposed that included a clinician-
administered tool for widespread pain index (WPI) and the symptom severity (SS)
scale of key characteristic signs and symptoms
• There is a strong genetic and familial component to the development of
fibromyalgia.
• Family members of fibromyalgia patients:
• irritable bowel syndrome, temporomandibular disorders, headaches, and a host of other
regional pain syndromes.
• higher concentrations of substance P and glutamate in cerebral spinal fluid (CSF)
compared with normal controls

23. Fibromyalgia
• Opioidergic activity is normal or increased
• High levels of CSF enkephalins
• Lower CSF level of 3-methoxy-4-hydroxyphenethylene glycol (MPHG) – principal
metabolite of NE

24. Treatment
• Pharmacologic
• two serotonin and
norepinephrine receptor
inhibitors (SNRIs) (duloxetine
and milnacipran),
• pregabalin,
• amitriptyline,
• gabapentin,
• gamma-hydroxybutyrate
(sodium oxybate)
• Non-Pharmacologic
• patient education,
• supportive therapy,
• exercise programs (specifically
low-intensity low-impact
programs),
• cognitive-behavioral and
operant-behavioral therapy

25. NEUROPATHIC PAIN
SYNDROMES

26. Neuropathic Pain Syndromes
Herpes Zoster and Postherpetic Neuralgia
Diabetic Painful Neuropathy
Complex Regional Pain Syndrome
Human Immunodeficiency Virus Neuropathy
Phantom Pain

27. Herpes Zoster and Postherpetic Neuralgia
• Acute herpes zoster - prodrome of dermatomal pain before the skin eruptions
• About 10% to 15% of patients (30% to 50% in the elderly) develop postherpetic
neuralgia (PHN), or pain that persists more than 3 months after resolution of the
rash
• Risk Factors: increased pain during the acute stage, greater severity of the skin
lesion, older age, and the presence of a prodrome
• Antiviral drugs (acyclovir, famciclovir, or valacyclovir) - hastens the healing of the
rash, reduce the duration of viral shedding, and decrease the incidence of PHN

28. Treatment
• Mainstay treatment: anticonvulsants, opioids, and antidepressants
• Gabapentin and pregabalin
• DOC when quality of life, side effects, prevention of addiction, and regulatory issues are
considered important in addition to pain relief
• Side effects: somnolence, dizziness, and peripheral edema
• Nortriptyline is preferred over amitriptyline
• Side effects of antidepressants: tachycardia, dry mouth, constipation, and symptoms
of prostatism in elderly males
• Treatment of choice for neuropathic pain syndromes based on efficacy:
• Antidepressants > opioids > tramadol > gabapentin/pregabalin

29. Treatment
• Lidocaine patch – for allodynia
• Capsaicin 8% topical patch – for localized pain
• Interventional techniques
• Intrathecal methylprednisolone, 60 mg in lidocaine, given once a week for four times
• Intrathecal alcohol
• Spinal cord stimulation (SCS)

30. Diabetic Painful Neuropathy
• Peripheral neuropathy - approximately 65% of patients with insulin-dependent
diabetes
• Distal symmetric polyneuropathy – most common
• Median nerve mononeuropathy - wrist
• Visceral autonomic neuropathy
• Pathophysiology - includes the polyol pathway, microvascular, and glycosylation
end-product theories  CHRONIC ISCHEMIA OF THE NERVE

31. Treatment
• Tight control of the patient ’s blood glucose
• Pharmacologic therapy:
• Gabapentin and Pregabalin - effective in the management of DPN,
• The efficacy of gabapentin is enhanced by the addition of controlled-release morphine or
nortriptyline
• TCA
• SSRI – not as effective
• Serotonin–norepinephrine reuptake inhibitors (Duloxetine, Milnacipran) – first-choice
drugs
• Opioids, Tramadol

32. Complex Regional Pain Syndrome
• CRPS type I – originally termed reflex sympathetic dystrophy
• CRPS type II – causalgia; preceded by a nerve injury
• Risk factors:
• previous trauma, nerve injury (for causalgia), previous surgery, work-related injuries, and
female sex
• Signs and symptoms:
• spontaneous pain, hyperalgesia, allodynia, plus trophic, sudomotor, vasomotor
abnormalities, and, finally, active and passive movement disorders.

33. Treatment
• Sympathetic nerve blocks
• Physical therapy
• Medications
• Oral therapy : Gabapentin, Memantine (an NMDA blocker), and Alendronate
• IV infusions: Ketamine and Bisphosphonates
• Ketamine can be given either as a 4- to 5-day infusion at 1 to 7 μg/kg/min (5 to 30 mg/hr in a 70-
kg patient) or for 4 hours daily for 10 days at an infusion rate of 0.35 mg/kg/hr (24 mg/hr in a 70-
kg person).
• Intramuscular or subcutaneous calcitonin
• SCS should be considered if the patient does not respond to any of these treatments.

34. Human Immunodeficiency Virus Neuropathy
• Symptomatic neuropathy occurs in 10% to 35% of patients
• Sensory neuropathies associated with HIV include
• Distal Sensory Polyneuropathy - more common neuropathy related to the viral
infection
• Antiretroviral Toxic Neuropathy (ATN) - secondary to treatment
• Clinical features: painful allodynia and hyperalgesia
• Onset is gradual and most commonly involves the lower extremities
• Neuropathy and dysesthesia progress from the distal to the more proximal
structures
• Minimal subjective or objective motor involvement - limited to the intrinsic
muscles of the foot

35. Treatment
• Treatment is symptomatic and includes optimization of the patient’s metabolic
and nutritional status
• Cessation or dose reduction of treatment with nucleoside reverse transcriptase
inhibitors
• Anticonvulsants - Lamotrigine (300 mg/day)
• Gabapentin - 1,200 to 3,600 mg/day

36. Phantom Pain
• 60% of patients with amputated extremities experience nonpainful sensations in
the absent, phantom limb
• Onset: immediate but commonly occurs within the first few days following
amputation
• Phantom pain is caused by both peripheral and central factors
• Peripheral mechanisms - include neuromas, an increase in C-fiber activity, and
sodium channel activation.
• Central mechanisms - include abnormal firing of spinal internuncial neurons and
supraspinal involvement secondary to the development of new synaptic connections in
the cerebral cortex.

37. Treatment
• Prophylactic measures:
• perioperative epidural infusions of opioids and local anesthetics or clonidine
• continuous brachial plexus blockade with Memantine
• Pharmacologic measures:
• Gabapentin, Morphine, Tramadol, Intramuscular Botulinum toxin, and epidural
Ketamine
• Nonpharmacologic measures:
• Transcutaneous electrical nerve stimulation, Spinal cord stimulators, and Biofeedback
• Most effective approach: Combination of pharmacologic treatment with
physical, psychological, or behavioral intervention

38. CANCER PAIN

39. Cancer Pain
• 25% of patients in active treatment
• 90% of patients with advanced cancer
• can be Somatic, Visceral, or Neuropathic
• Somatic pain – opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), or
cyclooxygenase 2 inhibitors, and is also amenable neural blockade
• Visceral pain – sympathetic nerve blocks
• Neuropathic pain – anticonvulsants, opioids, TCAs, serotonin–norepinephrine
reuptake inhibitors, or combinations of these drugs.

40. Treatment
1. Appropriate tumor-specific antineoplastic therapy
2. Pain medications
3. Interventional management
4. Behavioral and psychological management
5. Hospice care
• Pharmacologic therapies – opioids, antidepressants, anticonvulsants, NSAIDs, corticosteroids,
oral local anesthetics, and topical analgesics.
• Opioids – mainstay of treatment for cancer pain
• Interventional treatments – neurolytic sympathetic nerve blocks and intrathecal opioids.
• Vertebroplasty or kyphoplasty – vertebral compression syndromes

41. Neurolytic Blocks for
Visceral Pain from Cancer

42. Neurolytic Blocks for Visceral Pain from
Cancer
Celiac Plexus Block
Superior Hypogastric Plexus
Block
Ganglion Impar Block

43. Celiac Plexus Block
Location: 1 cm anterior to
the anterior and
upper border of L1
 Fifty percent alcohol or
6% to 10% phenol
 Dosage
 30 to 40 mL –
retrocrural and
anterocrural
approach
 10 to 15 mL on each
side – splanchnic
nerve blockade

44. Complications
• Orthostatic hypotension, back pain, retroperitoneal hematoma,
reactive pleurisy, hiccups, hematuria, transient diarrhea, abdominal
aortic dissection, transient motor paralysis, paraplegia
• Transient motor paralysis and Paraplegia - due to spasm of the
lumbar segmental arteries that perfuse the spinal cord, direct
vascular or neurologic injury, or retrograde spread to the nerve roots
or spinal cord

45. Superior Hypogastric Plexus Block
 Location: L5-S1
intervertebral disc
space
 6 to 8 mL of local
anesthetic is used for
a diagnostic block
 phenol or alcohol –
neurolysis

46. Ganglion Impar Block
 Four to 8 mL of local
anesthetic – diagnostic
block
 8% to 10% phenol or 50%
alcohol – neurolysis

47. Pharmacologic Management
of Pain

48. Opioids
• Morphine – standard for opioid therapy for cancer pain
• The numbers needed to treat or NNT for 10 mg of morphine for postoperative pain
is 2.9 and its numbers needed to harm or NNH is 9.1.
• Hydromorphone - μ-receptor agonist, is three to five times more potent than
morphine when given orally and five to seven times more potent when given
parenterally.
• Pruritus, sedation, nausea, and vomiting occur less frequently compared with morphine
• Hydromorphone-3-glucoronide, lacks analgesic property but possesses properties
similar to that of morphine-3-glucuronide

49. Opioids
• Methadone – 60% to 95% bioavailability, high potency, and a long duration of
action
• Lacks an active metabolite with an additional salutary effects such as acting as an NMDA
receptor antagonist and serotonin reuptake inhibitor
• Inexpensive
• long and unpredictable half-life of 8 to 80 hours
• Side effects: cardiac rhythm abnormalities, including QT prolongation and Torsade de
pointes

50. Opioids
• Oxycodone
• mainly a prodrug
• Active form: Oxymorphone (a μ-opioid agonist)
• Inactive metabolite: Noroxycodone
• NNT of 2.5 in neuropathic pain
• greater affinity to the μ-receptor than morphine and has little or no affinity to the κ-
opioid receptor
• 10 times more potent than morphine when given intravenously
• Low histamine release
• Rapid onset – due to its greater lipid solubility

51. Opioids
• Buprenorphine
• Partial agonist at the μ-receptor, a κ-antagonist, and a weak δ-agonist
• Rapid onset (30 minutes) when given orally
• Long duration of action – 6 to 9 hours
• antagonizes the opioid effects of full agonists such as morphine or hydromorphone due
to its partial opioid agonist pharmacodynamics.
• Weak opioids:
• Codeine, hydrocodone, tapentadol, and tramadol

52. Opioids
• Codeine
• transformed to morphine via the enzyme cytochrome P450 2D6
• NNT of 16.7
• 9% of Caucasians do not have the enzyme and do not experience analgesia from codeine
• Asians have a lower rate of codeine O-demethylation, resulting in less morphine
formation
• Hydrocodone
• peak serum concentration: within 1 to 2 hours
• half-life: 2.5 to 4 hours
• An additive effect is noted when combined with ibuprofen

53. Opioids
• Tramadol
• weak opioid agonist and a monoaminergic drug
• NNTs of 8.5 for 50 mg, 5.3 for 75 mg, 4.8 for 100 mg, and 2.9 for 150 mg
• maximum dose: 400 to 500 mg/day
• Tapentadol
• Dual mode of action: μ-opioid agonist and a norepinephrine reuptake inhibitor
• Modestly stronger than tramadol
• for moderate-to-severe acute pain,
• extended-release formulation – moderate-to-severe chronic pain and diabetic
neuropathy

54. Opioids
• Oral equianalgesic doses of morphine 10 mg intravenously or 30 mg orally are
1. 200 mg of codeine
2. 30 mg of hydrocodone
3. 20 mg of oxycodone
4. 150 mg of tramadol
5. 75 mg of tapentadol.
• Opioids are commonly used for cancer pain, with long-acting opioids
supplemented by short-acting ones for breakthrough pain

55. Pharmacologic Treatments
of Neuropathic Pain

56. Pharmacologic Treatments of Neuropathic
Pain
• First-line medications
• Gabapentin, Pregabalin, SNRIs, and TCAs
• Second-line medications
• Capsaicin 8% patches, Lidocaine patches, and Tramadol
• Third-line medications
• Botulinum toxin A and Opioids

57. Antidepressants (TCAs)
• Serotonergic effect (interference with serotonin reuptake and alteration of
serotonin binding to receptors in neural tissue)
• Noradrenergic effect (interaction with α-receptors)
• Opioidergic effect
• Blockade of the NMDA receptor complex
• Inhibition of the uptake of adenosine
• Blockade of sodium and calcium channels
• Also have an anti-inflammatory effect in animal models of pain

58. Antidepressants (SNRIs)
• block the reuptake of serotonin and norepinephrine,
• Duloxetine having increased selectivity for serotonin
• Venlafaxine has more serotonergic effects at lower doses but with greater
noradrenergic activity at higher dosages.
• Duloxetine and Milnacipran
• preferential noradrenergic effect, have longer half-lives (12 and 8 hours respectively), and
have no active metabolites

59. Antidepressants (SNRIs)
• SNRIs have an antinociceptive effect
• Duloxetine – DPN and fibromyalgia
• Milnacipran – fibromyalgia
• The efficacy of the SNRIs in DPN and fibromyalgia, coupled with the better side
effect profile (free of cholinergic, histaminic, and α-adrenergic receptor effects, and
less potential for drug interactions) in comparison to the TCAs, are probably the
reasons for their increased preferential usage

60. Side effects of antidepressants
• cholinergic effects – dry mouth, sedation, and urinary retention
• Venlafaxine – hypertension and mania, and may exacerbate seizures
• A gradual withdrawal is recommended for Duloxetine to prevent agitation, anxiety,
confusion, and hypomania
• TCAs – weight gain, impair driving ability during the first week

61. Anticonvulsants
• Neuropathic pain – associated with changes in sodium and calcium channel
subunit expression, resulting in functional changes
• Chronic nerve injury – redistribution and alteration of subunit compositions of
sodium and calcium channels  spontaneous firing at ectopic sites along the
sensory pathway
• Sodium channel blockers – inhibit spontaneous activities at neuromas, DRG,
and at the dorsal horn of the spinal cord
• Most anticonvulsants block sodium channels

62. Anticonvulsants
• Acts on ion channel systems
• GABA-A receptor agonists (topiramate and felbamate), GABA-A transaminase blockers
(vigabatrin), GABA-A transport blockers (tiagabine), and glutamate receptor antagonists
(felbamate and topiramate)
• Directly block calcium channels (lamotrigine), T-type calcium channels
(topiramate and zonisamide) and α2-delta subunits (gabapentin and pregabalin).
• Randomized controlled studies demonstrate the efficacy of the anticonvulsants in
several neuropathic pain syndromes including trigeminal neuralgia, PHN, DPN,
HIV polyneuropathy, phantom limb pain, spinal cord injury (SCI) pain, and central
poststroke pain.

63. Anticonvulsants
• Gabapentin
• effective drug in neuropathic pain (PHN, DPN, and SCI), multiple sclerosis pain,
neuropathic cancer pain, and fibromyalgia
• Median effective dose is 900 to 1,800 mg/day.
• Pregabalin
• Maximum dose
• 600 mg/day in patients with creatinine clearance more than 60 mL/min
• 300 mg in patients with clearance of 30 to 60 mL/min

64. Anticonvulsants
• Lamotrigine
• Effective in HIV polyneuropathy, pain from SCI, trigeminal neuralgia, and central
poststroke pain
• The most common side effect is rash, and use of lamotrigine is limited by the risk of
Stevens–Johnson syndrome
• Topiramate
• effective in migraine prophylaxis, similar to Divalproex
• Oxcarbazepine
• effective in trigeminal neuralgia with fewer side effects
• analgesic effect is fast and pain relief may be noted within 24 to 48 hours

65. Side effects of anticonvulsants
• dizziness,
• fatigue,
• somnolence,
• weight gain,
• peripheral edema (gabapentin and
pregabalin);
• Rash (lamotrigine)
• paresthesia,
• cognitive effects,
• weight loss (topiramate);
• Hyponatremia
• low thyroid concentrations
(oxcarbazepine)

67. Lidocaine Patch
• 5% lidocaine patch – analgesia is by local sodium channel blockade and not by its
systemic effects
• contains 700 mg of lidocaine inside an adhesive
• maximum of three patches is applied for a maximum of 12 hr/day
• 16 to 18 hours – for patients who continue to have pain when the patch is removed
• a 2-week trial period is recommended
• only about 3% of the total dose applied is absorbed systemically
• maximum plasma lidocaine concentration is usually achieved on the second day of a 12-
hours-per-day patch application
• can be used effectively for patients with PHN

68. Capsaicin Patch
• Capsaicin – defunctionalize TRPV1 nerve endings and reduce epidermal nerve
fiber density
• The higher-concentration capsaicin 8% patch (Qutenza, Acorda Therapeutics) has been
shown to be better than placebo and better than low-concentration (0.04%) capsaicin
• effective in PHN, DPN, and HIV neuropathy
• Causes burning sensation  local anesthetic cream is applied 60 minutes before the
patch is applied for 60 to 90 minutes
• There is an increase in pain 20 to 30 minutes after application, which disappears 2 to 3
hours after removal of the patch.
• Relief can be up to 12 weeks after one application.
• A maximum of four doses can be given at intervals of 12 weeks

69. Mexiletine, and Intravenous Lidocaine
• Mexiletine
• oral analogue of lidocaine
• used for diabetic neuropathy, thalamic stroke pain, spasticity, and myotonia but has been
shown to only have modest efficacy
• Its efficacy is similar to that of intravenous lidocaine
• Median recommended dose of mexiletine – 600 mg/per day.

70. Cannabinoids
• Cannabis
• has been studied for treating neuropathic pain
• Nabiximol – a cannabinoid-based oral mucosal spray, were negative for the primary
outcome of 50% pain reduction
• Cannabinoids were therefore given a weak recommendation against use
• Inhaled (smoked) cannabis for treatment of chronic neuropathic pain showed an NNT
for short-term reduction in neuropathic pain similar to that of TCAs, SNRIs, and
gabapentin.
• Nabiximols, but not delta-9-tetrahydrocannabinol (THC), were modestly effective in the
treatment of cancer-related pain
• Dronabinol and Nabilone – synthetic cannabinoids approved for nausea treatment, had
no pain benefit in acute postsurgical pain clinical trials
• Dronabinol did improve pain intensity in chronic pain patients who were opioid tolerant

71. Buprenorphine–Naloxone Therapy
• Buprenorphine–naloxone (bup/nal in 4:1 ratio; Suboxone, Indivior Inc.)
• semisynthetic, sublingual tablet consisting of buprenorphine and naloxone in fixed 4:1
ratio
• effective in outpatient-based opioid addiction treatment and offers several advantages
over methadonem maintenance programs
• Has been shown to be effective in patients with chronic pain with opioid dependence or
addiction and not in those without

73. Interventional Techniques

74. Discography
• Symptoms of discogenic pain are nonspecific and include nonradicular back pain
that is worse in the sitting position and with lifting maneuvers
• neurologic examination – usually normal
• MRI may show a high-intensity zone on the T2 sagittal images, indicating an
annular tear
• Treatment: stabilization, core strengthening, exercise training, back education,
activity modification, and occasional ESIs for managing symptom exacerbation
• Diagnostic discography remains a useful tool in identifying painful
intervertebral discs.

75. Indications for Diagnostic Discography
1. Evaluation of abnormal discs to assess the extent of abnormality or correlation of
the abnormality with clinical symptoms
2. Assessment of patients with persistent severe symptoms in whom diagnostic
tests have failed to reveal which suspected disc is the source of pain,
3. Assessment of discs before fusion to determine which discs within the proposed
fusion segment are symptomatic
4. Confirmation of a contained disc herniation or investigation of contrast
distribution pattern before intradiscal procedures.

76. Discography
• can be performed on an outpatient basis with fluoroscopic guidance, under light
sedation
• Antibiotic prophylaxis – either intradiscally or intravenously
• Nonionic contrast is injected into the disc
• The patient is asked to rate his or her pain on a 0 to 10 scale before and during
injection, and whether the pain is concordant, that is, similar to the pain for which
the patient is being evaluated

77. Discography
• The suggested end points for injection include
(1) pain severity of 6 out of 10 or greater,
(2) intradiscal pressure of less than 50 psi above opening pressure, or
(3) a total of less than 3.5 mL of contrast medium has been injected
• Anteroposterior and lateral images are taken
• After recovery, the patient is sent for a postdiscography computed tomography
(CT) scan, preferably within 4 hours of the discography

78. Discography
• Discitis – most feared complication of discography
• Diagnosis:
• worsening back pain the week after discography, and elevated erythrocyte sedimentation
rate and C-reactive protein that usually peaks 53 weeks after the procedure
• Staphylococcus aureus – most common cause

79. Thermal Annular Procedures
• Intradiscal electrothermal therapy (IDET)
• Thermal resistance catheter is placed percutaneously in the posterolateral portion of the
disc.
• Heat causes the collagen of the annulus fibrosis to contract.

80. Minimally Invasive Lumbar Decompression
Procedure
• Spinal stenosis – narrowing of the spinal canal with compression of the nerve
roots
• can be secondary to hypertrophy of the ligamentum flavum or the facet joint
• Location of low back pain: low back area, buttocks, thighs, and/or legs
• Can be in combination with neurogenic claudication, especially with erect posture (due
to smaller spinal canal diameter in this position) or walking
• MILD procedure – minimally invasive method of spinal decompression
• Indicated in patients with: low back pain and neurogenic claudication associated
with MRI or CT evidence of central canal stenosis secondary to ligamentum flavum
hypertrophy in the lumbar segments.
• The procedure involves limited percutaneous laminotomy and thinning of the
ligamentum flavum to increase the critical diameter of the stenosed spinal canal.

81. Vertebroplasty and Kyphoplasty
• are percutaneous interventional modalities to treat vertebral compression fractures
• VCFs - a condition usually secondary to osteoporosis in elderly patients
• The pain is usually a deep back pain and there may be intercostal neuralgic symptoms or
radiculitis and paravertebral muscle spasm.
• Pain is relieved by bed rest and the recumbent position.
• Radiography shows osteopenia or decreased bone mass
• MRI is the imaging modality of choice

82. Vertebroplasty and Kyphoplasty
• Vertebroplasty - injection of polymethylmethacrylate (PMMA) into the affected
vertebral body
• Kyphoplasty - percutaneous insertion of a balloon into the vertebral body,
infalation of the balloon and filling it with PMMA, prior to the injection of the
cement
• 2 ml of cement can be adequate
• The patient remains supine for 3 to 5 hours after the procedure
• CT scan is performed afterward – assess for cement distribution and complications
such as bleeding and leakage of the cement

83. Vertebroplasty and Kyphoplasty
• Complications:
• Cement leakage – due to level of injection, severity of fracture, and the amount of
cement injected
• Neurologic complications - radiculopathy, spinal claudication, and paraplegia
• Complications related to the procedure - infection, bleeding, and allergic reactions from
the PMMA or contrast medium.

84. Spinal Cord Stimulation
• Analgesic effect involves the gate control theory, neurotransmitter modulation in
the spinal cord affecting pain pathways and suppression of sympathetic activity,
antidromic and activity supraspinal mechanisms
• increases the input of the large nerve fibers, thus closing the “gate” at the
substantia gelatinosa of the dorsal horn of the spinal cord
• alter the local neurochemistry at the dorsal horn  decrease of the
hyperexcitability of the wide dynamic neurons
• increased levels of GABA and a decrease in glutamate and aspartate
• Ischemic pain – the analgesia may be secondary to alteration of the sympathetic
tone with restoration of a favorable oxygen supply-and-demand balance

85. Spinal Cord Stimulation
• Clinical indications:
• Post laminectomy syndrome or failed back surgery syndrome (FBSS),
• CRPS
• Neuropathic pain syndromes
• Angina
• Chronic critical limb ischemia and pain
• Contraindications: systemic or local site of infection and abnormal coagulopathy
• Complications: nerve and SCI, infection, hematoma, and lead breakage or
migration.

86. Peripheral Nerve Stimulation
• can be used to treat neuropathic pain, ideally arising from a single nerve
• it is important to distinguish between open and percutaneous PNS approaches
• OPEN PNS:
• nerve stimulation is made feasible with a circumferential (cuff) electrode that requires a
surgical exposure of the target nerve, then application of high frequency (10 kHz)
alternating current using a cuff electrode
• PERCUTANEOUS PNS:
• involves the use of cylindrical percutaneous lead (originally designed for SCS) in close
proximity to the target nerve or in the subcutaneous field area supplied by the target
nerve

87. Peripheral Nerve Stimulation
• Indications:
• focal neuropathic pain such as occipital neuralgia, facial neuralgias, and PHN
• refractory angina,
• abdominal pain,
• pelvic pain,
• knee pain after arthroplasty
• low back pain (in combination with SCS)

88. Dorsal Root Ganglion Stimulation
• A hybrid between SCS and PNS
• special percutaneous leads are introduced, initially in the interlaminar epidural
space, and directed toward the adjacent target DRG
• Advantages
• targeting unique dermatomes and difficult-to-target areas, such as the foot,
• minimal-to-no positional changes in paresthesia intensity

89. Occipital Nerve Stimulation
• a form of peripheral nerve field stimulation where there is inhibition of central
nociceptive impulses by stimulation of the superficial nerve branches of C2 and
C3.
• Provides reversible and effective therapy for intractable headache

90. Intrathecal Drug Delivery (IDD)
• enables opioid to be directly deposited near the spinal cord receptors, resulting in
analgesia at lower doses;
• Additional mechanism: release of adenosine in the CSF
• Major Indications: cancer pain and pain of spinal origin
• 2 medications approved by the FDA for IDD:
• preservative-free morphine
• synthetic peptide ziconotide
• First-line agents: Morphine, hydrocodone, or ziconotide
• Off-label meds: hydromorphone, fentanyl, the local anesthetic bupivacaine, and
clonidine

91. Intrathecal Drug Delivery (IDD)
• Side effects: pruritus, urinary retention, and peripheral edema, intrathecal
catheter tip granuloma
• Granuloma formation – increased with higher doses and concentrations of
morphine and hydromorphone but not fentanyl
• A trial can be performed intrathecally or through the epidural space, by a single
shot, intermittent bolus, or a continuous infusion

92. Intrathecal Drug Delivery (IDD)

93. Complications of Intrathecal Drug Delivery
(IDD)
• Procedure/device-related
complications
• wound dehiscence
• Skin erosion over the device
• Infection
• Bleeding
• CSF leak
• seroma or hygroma collection
• pump malfunction
• catheter kink or shear.
• Opioid-related complications
• androgen deficiency
• decreased testosterone levels and
hypogonadism with increased risk
of bone mineral deficiency,
• Peripheral edema with morphine
and hydromorphone,
• Pruritus
• urinary retention
• formation of an intrathecal
granuloma
• Bupivacaine
• Sensorimotor deficits
• urinary retention
• Clonidine
• hypotension

94. • End 